Tag Archives: Gary Taubes

Book Review: Why We Get Fat

Gary Taubes’ latest book is Why We Get Fat: And What To Do About It. I give it five stars per Amazon.com’s ranking system (I love it).

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At the start of my medical career over two decades ago, many of my overweight patients were convinced they had a hormone problem causing it. I carefully explained that’s rarely the case. As it turns out, I may have been wrong. And the hormone is insulin.

Mr. Taubes wrote this long-awaited book for two reasons: 1) to make the ideas in his 2007 masterpiece (Good Calories, Bad Calories) more accessible to the public, and 2) to speed up the process of changing conventional wisdom on overweight. GCBC was the equivalent of a college-level course on nutrition, genetics, history, politics, science, physiology, and biochemistry. Many nutrition science geeks loved it while recognizing it was too difficult for the average person to digest.

Paradigm Shift

The author hopes to convince us that “We don’t get fat because we overeat; we overeat because we’re getting fat.” We need to think of obesity as a disorder of excess fat accumulation, then ask why the fat tissue isn’t regulated properly. A limited number of hormones and enzymes regulate fat storage; what’s the problem with them?

Mr. Taubes makes a great effort convince you the old “energy balance equation” doesn’t apply to fat storage. You remember the equation: eat too many calories and you get fat, or fail to burn up enough calories with metabolism and exercise, and you get fat. To lose fat, eat less and exercise more. He prefers to call it the “calories-in/calories-out” theory. He admits it has at least a little validity. Problem is, the theory seems to have an awfully high failure rate when applied to weight management over the long run. We’ve operated under that theory for the last half century, but keep getting fatter and fatter. So the theory must be wrong on the face of it, right? Is there a better one?

So, Why DO We Get Fat?

Here is Taubes’s explanation. The hormone in charge of fat strorage is insulin; it works to make us fatter, building fat tissue. If you’ve got too much fat, you must have too much insulin action. And what drives insulin secretion from your pancreas? Dietary carbohydrates, especially refined carbs such as sugars, flour, cereal grains, starchy vegetables (e.g., corn, beans, rice, potatoes), liquid carbs. These are the “fattening carbs.” Dozens of enzymes and hormones are at play either depositing fat into tissue, or mobilizing the fat to be used as energy. It’s an active process going on continously. Any regulatory derangement that favors fat accumulation will CAUSE gluttony (overeating) or sloth (inactivity). So it’s not your fault.

What To Do About It

Cut back on carb consumption to lower your fat-producing insulin levels, and you turn fat accumulation into fat mobilization.

Before you write off Taubes as a fly-by-night crackpot, be aware that he’s received three Science-in-Society Journalism Awards from the National Association of Science Writers. He’s a respected, professional science writer. Having read two of his books, it’s clear to me he’s very intelligent. If he’s got a hidden agenda, it’s well hidden.

One example illustrates how hormones control growth of tissues, including fat tissue. Consider the transformation of a skinny 11-year-old girl into a voluptuous woman of 18. Various hormones make her grow and accumulate fat in the places we now see curves. The hormones make her eat more, and they control the final product. The girl has no choice. Same with our adult fat tissue, but with different hormones. If some derangement is making us grow fatter, it’s going to make us more sedentary (so more energy can be diverted to fat tissue) or make us overeat, or both. We can’t fight it. At not least very well, as you can readily appreciate if look at the people around you at any American shopping mall.

This’N’That

Taubes’s writing is clear and persuasive. He doesn’t beat you over the head with his conclusions. He lays out a logical series of facts and potential connections and explanations, helping you eventually see things his way. If insulin controls fat storage by building and maintaining fat tissue, and if carboydrates drive insulin secretion, then the way to reduce overweight and obesity is carbohydrate-restricted eating, especially avoiding the fattening carbohydrates. I’m sure that’s true for many folks, perhaps even a majority.

If you’re overweight and skeptical about this approach, you could try out a very-low-carb diet for a couple weeks or a month at little expense and risk (but not zero risk). If Mr. Taubes and I are right, there’s a good chance you’ll lose weight. At the back of the book is a university-affiliated low-carb eating plan.

If cutting carb consumption is so critical for long-term weight control, why is it that so many different diets—with no focus on carb restriction—seem to work, if only for the short run? Taubes suggests it’s because nearly all diets reduce carb consumption to some degree, including the fattening carbs. If you reduce your total daily calories by 500, for example, many of those calories will be from carbs. Simply deciding to “eat healthy” works for some people: stopping soda pop, candy bars, cookies, desserts, beer, etc. That cuts a lot of fattening carbs right there.

Losing excess weight or controlling weight by avoiding carbohydrates was the conventional wisdom prior to 1960, as documented by Mr. Taubes. Low-carb diets for obesity date back almost 200 years. The author attributes many of his ideas to German internist Gustav von Bergmann (1908).

Taubes discusses the Paleolithic diet, mentioning that the average paleo diet derived about a third of total calories from carbohdyrates (compared to the standard American diet’s 55% of calories from carb). My prior literature review found 40-45% of paleo diet calories from carbohydrate. I’m not sure who’s right.

Minor Bone of Contention RE: Coronary Heart Disease

Mr. Taubes provides numerous scientific references to back his assertions. I checked out one in particular because it didn’t sound right. Some background first.

Reducing our total fat and saturated fat consumption over the last 40 years was supposed to lower our LDL cholesterol, thereby reducing the burden of coronary heart disease, which causes heart attacks. Instead, we’ve experienced the obesity epidemic as those fats were replaced by carbohydrates. Taubes mentions a 2009 medical journal article by Kuklina et al, in which Taubes says Kuklina points out the number of heart attacks has not decreased as we’ve made these diet changes. Kuklina et al don’t say that. In fact, age-standardized heart attack rates have decreased in the U.S. during the last decade.

Furthermore, autopsy data document a reduced prevalence of anatomic coronary heart disease in people aged 20-59 from 1979 to 1994, but no change in prevalence for those over 60. The incidence of coronary heart disease decreased in the U.S. from 1971 to 1998 (the latest reliable data). Death rates from heart disease and stroke have been decreasing steadily over the last 40 years in the U.S.; coronary heart disease death rates are down by 50%. I do agree with Taubes that we shouldn’t credit those improvements to reduced total and saturated fat consumption. [Reduced trans fat consumption may play a role, but that’s off-topic.]

I think Mr. Taubes would like to believe that coronary artery disease is either more severe or unchanged in the last few decades because of low-fat, high-carb eating. That would fit nicely with some of his theories, but it’s not the case. Coronary artery disease is better now thanks to a variety of factors, but probably not diet (setting aside the trans-fat issue).

Going Forward

Low-carb dieting was vilified over the last half century partly out of concern that the accompanying high fat consumption would cause premature heart attacks, strokes, and death. We know now that total dietary fat and saturated fat have little to do with coronary heart disease and atherosclerosis (hardening of the arteries), which sets the stage for a resurgence of low-carb eating.

I advocate Mediterranean-style eating as the healthiest, in general. It’s linked with prolonged life and lower risk of heart disease, stroke, dementia, diabetes, and cancer. On the other hand, obesity is a strong risk factor for premature death and development of heart disease, stroke, diabetes, and cancer. If consistent low-carb eating cures the obesity, is it healthier than the Mediterranean diet? Maybe so. Would a combination of low-carb and Mediterranean be better? Maybe so. I’m certain Mr. Taubes would welcome a decades-long interventional study comparing low-carb with the Mediterranean diet. But that’s probably not going to happen in our lifetimes.

Gary Taubes rejects the calories-in/calories-out theory of overweight that hasn’t done a very good job for us over the last 40 years. Taubes’s alternative ideas deserve serious consideration.

Steve Parker, M.D.

References:

Coronary heart disease autopsy data: American Journal of Medicine, 110 (2001): 267-273.

Reduced heart attacks: Circulation, 12 (2010): 1,322-1,328.

Reduced incidence of coronary heart disease: www.UpToDate.com, topic: “Epidemiology of Coronary Heart Disease,” accessed December 11, 2010.

Death rates for coronary heart disease: Journal of the American Medical Association, 294 (2005): 1,255-1,259.

Disclosure: I don’t know Gary Taubes. I requested from the publisher and received a free advance review copy of the book. Otherwise I received nothing of value for this review.

Disclaimer: All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status. Always consult your personal physician before making any dietary or exercise changes.

Update April 22, 2013:

As mentioned above, WWGF was based on Taubes’ 2007 book, Good Calories, Bad Calories. You may be interested in a highly critical review of GCBC by Seth at The Science of Nutrition.

Competing Theories of Overweight and Obesity

God, help us figure this out

A few months ago, several of the bloggers/writers I follow were involved in an online debate about two competing theories that attempt to explain the current epidemic of overweight and obesity. The theories:

  1. Carboydrate/Insulin (as argued by Gary Taubes)
  2. Food Reward (as argued by Stephan Guyenet)

The whole dustup was about as interesting to me as debating how may angels can dance on the head of pin.

Regular readers here know I’m an advocate of the Carboydrate/Insulin theory. I cite it in Conquer Diabetes and Prediabetes: The Low-Carb Mediterranean Diet and The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer (2nd edition). But the Food Reward theory also has validity. They’re both right, to an extent. They’re not mutually exclusive. The Food Reward theory isn’t as well publiziced as Carbohydrate/Insulin.

Dr. Guyenet lays out a masterful defense of the Food Reward theory at his blog. Mr. Taubes presents his side here, here, here, here, and here. If you have a couple hours to wade through this, I guess I’d start with Taubes’ posts in the order I list them. Finish with Guyenet.

You’d think I’d be more interested in this. I’m still not.

Moving from theory to real world practicality, I do see that limiting consumption of concentrated refined sugars and starches helps with loss of excess body fat and prevention of weight regain. Not for everbody, but many. Whether that’s mediated through lower insulin action or through lower food reward, I don’t care so much.

Steve Parker, M.D.

h/t Dr. Emily Deans

Are Saturated Fats Really All That Bad?

This is an epic post of mine from the old Advanced Mediterranean Diet blog, originally dated July 6, 2009.  That was a watershed year for me because of the ideas in this article.

I’ve been thinking a lot lately about saturated fats. Weird, huh?

No saturated fat in grapes

The American Heart Association recommends that Americans limit the amount of saturated fats they eat to less than 7 percent of total daily calories. If you eat 2,000 calories a day, no more than 140 of them should come from saturated fats. That’s about 16 grams of saturated fats.

In over two decades of clinical practice, I’ve never run across a patient willing to do that calculation. Not many physicians could tell you the “seven percent rule.”

One of the two major themes of Gary Taubes’ book, Good Calories, Bad Calories, is that dietary saturated fats are not particularly harmful to our health, if at all. From what I’ve been taught, this is sacrilegious. “Saturated fats are a major cause of heart disease and strokes,” I’ve heard and read over and over. In brief, this is the Diet-Heart Hypothesis or the “lipid hypothesis”: Dietary saturated fat, total fat, and cholesterol are directly related to coronary heart disease and other forms of atherosclerosis (aka hardening of the arteries).

In his review of Taubes’ book, Dr. George Bray didn’t even address Taubes’ point about saturated fats, writing instead, “read and decide for yourself.”

That started me thinking either that the Diet-Heart Hypothesis is indefensible or that Dr. Bray is lazy. I don’t think he’s lazy. Dr. Bray is a Grand High Pooh-Bah in the fields of obesity and nutrition.

The American Heart Association in 1957 recommended that polyunsaturated fats replace saturated fats.

U.S. public health recommendations in 1977 were to reduce fat intake to 30% of total calories to lower the risk of coronary heart disease. Slowly, some fats were replaced mostly with carbohydrates, highly refined ones at that. This shift tends to raise triglycerides and lower HDL cholesterol levels, which may themselves contribute to atherosclerosis. Current recommendations are, essentially, to keep saturated fatty acids as low as possible.

One concern about substituting carbohydrates for fats is that blood sugar levels rise, leading to insulin release from the pancreas, in turn promoting growth of fat tissue and potentially leading to weight gain. Some believe that the public health recommendation to reduce total fat (which led to higher carbohydrate intake) is the reason for the dramatic rise in overweight and diabetes we’ve seen over the last 30 years.

Note that if intake of saturated fats is inadequate, our bodies can make the saturated fats it needs from carbohydrates. These are generally the same saturated fats that are present in dietary fats of animal origin. The only exceptions are the two essential fatty acids: alpha-linolenic acid and linoleic acid.

Why would saturated fats be harmful? Apparently because they raise blood levels of cholesterol (including LDL cholesterol – “bad cholesterol”), which is thought to be a cause of atherosclerosis, which increases the risk of coronary heart disease and stroke. I don’t recall seeing any mention of a direct toxic effect of saturated fats (or fatty acids) on arterial walls, where the rubber meets the road. (Saturated fats are broken down in the small intestine to glycerol and fatty acids.)

Dietary saturated fats also raise HDL cholesterol – “good cholesterol” – although not to the degree they raise LDL.

You needed a break

Let’s not forget many other factors that cause, contribute to, or predict coronary heart disease and atherosclerosis: smoking, family history, high blood pressure, obesity, diabetes, oxidative stress, homocysteine level, systemic inflammation, high-glycemic index diets, C-reactive protein, lack of exercise, and others. I discussed dietary factorsin my April 14, 2009, blog post.

Often overlooked in discussion of dietary fat effects is the great variability of response to fats among individuals. Response can depend on genetics, sex, fitness level, overweight or not, types of carbohydrates eaten, amount of total dietary fat, etc. And not all saturated fats affect cholesterol levels.

Many of the journal articles listed as references below support the idea that the link between dietary saturated fats and coronary heart disease is not strong, and may be nonexistent. Read them and you’ll find that:

  • Some studies show no association between dietary saturated fats and coronary heart disease.
  • Some studies associate lower rates of coronary heart disease with higher saturated fat intake.
  • Higher saturated fat intake was associated with less progression of coronary atherosclerosis in women.
  • Lowering saturated fat intake did not reduce total or coronary heart disease mortality.

“Read and decide for yourself,” indeed. I think you’ll begin to question the reigning dogma.

For example, here’s a conclusion from the Hooper article (from 2001):

In this review we have tried to separate out whether changes in individual fatty acid fractions are responsible for any benefits to health (using the technique of meta-regression). The answers are not definitive, the data being too sparse to be convincing. We are left with a suggestion that less total fat or less of any individual fatty acid fraction in the diet is beneficial.

And a conclusion of the J.B. German article:

At this time [2004], research on how specific saturated fatty acids contribute to coronary artery disease and on the role each specific saturated fatty acid play in other health outcomes is not sufficient to make global recommendations for all persons to remove saturated fats from their diet. No randomized clinical trials of low-fat diets or low-saturated fat diets of sufficient duration have been carried out; thus, there is a lack of knowledge of how low saturated fat intake can be without the risk of potentially deleterious health outcomes.

Zarraga and Schwartz (2006) conclude:

Numerous studies have been conducted to help provide dietary recommendations for optimal cardiovascular health. The most compelling data appear to come from trials that tested diets rich in fruits, vegetables, MUFAs [monounsaturated fatty acids], and PUFAs [polyunsaturated fatty acids], particularly the n-3 PUFAs. In addition, some degree of balance among various food groups appears to be a more sustainable behavioral practice than extreme restriction of a particular food group.

Here’s another of my favorite quotes on this topic, from the J.B. German article:

If saturated fatty acids were of no value or were harmful to humans, evolution would probably not have established within the mammary gland the means to produce saturated fatty acids . . . that provide a source of nourishment to ensure the growth , development, and survival of mammalian offspring.

Take-Home Points

The connection between dietary saturated fat and coronary heart disease is weak.

I may be excommunicated from the medical community for uttering this. You won’t hear it from most physicians or dietitians. They don’t have time to spend 80 hours on this topic, so they stick with the party line. And maybe I’m wrong anyway.

The scientific community is slowly moving away from the original Diet-Heart/Lipid Hypothesis. It is being replaced with stronger anti-atherosclerosis theories that promote:

  • fruit and vegetable intake
  • whole grain intake
  • low-glycemic index eating
  • increased consumption of plant oils and fish
  • moderate intake of nuts
  • ? moderate intake of low-fat diary (e.g., DASH diet) (less consensus on this point)

So, saturated fats and dietary cholesterol are being crowded out of the picture, or ignored. In many cases, saturated fats have literally been replaced by poly- and monounsaturated fats (plant oils). Several clinical studies indicate that’s a healthy change, but it may be related more to the healthfulness of the plant oils than to detrimental effects of saturated fats.

The original Diet-Heart Hypothesis won’t die until the American Heart Association and U.S. public health agencies put a gun to its head and pull the trigger. That will take another 10 years or more.

If you want to hedge your bets, go ahead and limit your saturated fat intake. It probably won’t hurt you. It might help a wee bit. By the same token, I’m not going on an all-meat and cheese, ultra-high-saturated fat diet; I don’t want to miss out on the healthy effects of fruits, vegetables, whole grains, fish, nuts, and low-glycemic index carbohydrates. Some would throw red wine into the mix. This “prudent diet” reflects what I hereby christen The 21st Century Diet-Heart Hypothesis.

If you’re worried about coronary heart disease and atherosclerosis, spend less time counting saturated fat grams, and more time on other risk-reducing factors: diet modification as above, get regular exercise, control your blood pressure, achieve a healthy weight, and don’t smoke. More bang for the buck.

What do you think?

Steve Parker, M.D.

Disclaimer: All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status. Always consult your personal physician before making any dietary or exercise changes.

Selected References Contradicting or Questioning the Diet-Heart Hypothesis (updated October 4, 2016):

Grasgruber, Pavel, et al. FOOD CONSUMPTION AND THE ACTUAL STATISTICS OF CARDIOVASCULAR DISEASES: AN EPIDEMIOLOGICAL COMPARISON OF 42 EUROPEAN COUNTRIES. Food & Nutrition Research 2016, 60: 31694 – http://dx.doi.org/10.3402/fnr.v60.31694 “Our results do not support the association between cardiovascular diseases and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link cardiovascular disease risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with cardiovascular diseases, these findings show that current dietary recommendations regarding cardiovascular diseases should be seriously reconsidered.”

Puaschitz, Nathalie, et al. Dietary Intake of Saturated Fat Is Not Associated With Risk of Coronary Events Or Mortality In Patients With Established Coronary Artery Disease. Journal of Nutrition, Feb. 1, 2015. First published online Dec. 10, 2014. doi: 10.3945/jn.114203505. The title of the article says it all. A strong majority (81%) of the 2412 study participants were men, so I’m not sure the results apply to women.

Chowdhury, Rajiv, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysisAnnals of Internal Medicine 2014;160(6):398-406-406. doi:10.7326/M13-1788  The conclusion of this meta-analysis: “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Ramsden, Christopher, et al.  Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.  British Medical Journal 2013; 346 doi: http://dx.doi.org/10.1136/bmj.e8707 (Published 5 February 2013). Cite this as: BMJ 2013;346:e8707  (Almost 500 middle-aged men with a recent coronary event were followed over time.  Those who substituted saturated fat with omega-6 fatty acid (polyunsaturated fatty acid, mostly linoleic acid) had higher death rates (cardiac and overall deaths) than those who continued their habitual diet.)  Also see editorial by Philip Calder in the same issue.

Astrup, A., et al (including Ronald Krause, Frank Hu, and Walter Willett). The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010. American Journal of Clinical Nutrition, 93 (2011): 684-688.  (The authors believe that replacing saturated fats with polyunsaturated fats (but not carbohydrates) can reduce the risk of coronary heart disease (CHD). For the last four decades, low-fat diets replaced fat with carbohydates. So they believe saturated fatty acids cause CHD or polyunsaturated fatty acids prevent it. I see no mention of total fat intake in this article written by major names in nutritional epidemiology and lipid metabolism. “In countries following a Western diet, replacing 1% of energy intake from saturated fatty acids with polyunsaturated fatty acids has been associated with a 2–3% reduction in the incidence of CHD.” “Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total saturated fatty acids because individual saturated fatty acids may have different cardiovascular effects and major saturated fatty acid food sources contain other constituents that could influence coronary heart disease risk.”)  A Feb. 19, 2012, press release from the Harvard School of Public Health covered much of the same ground. It’s titled “Time to Stop Talking About Low-Fat, say HSPH Nutrition Experts.”

Siri-Tarino, Patty, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition, January 13, 2010. doi:10.3945/ajcn.2009.27725

Skeaff, C. Murray and Miller, Jody. Dietary fat and coronary heart disease: Summary of evidence from prospective cohort and randomised controlled trials. Annals of Nutrition and Metabolism, 55 (2009): 173-201.

Halton, Thomas, et al. Low-carbohydrate-diet score and the risk of coronary heart disease in women. New England Journal of Medicine, 355 (2006): 1,991-2,002.

German, J. Bruce, and Dillard, Cora J. Saturated fats: What dietary intake? American Journal of Clinical Nutrition, 80 (2004): 550-559.

Ravnskov, U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. Journal of Clinical Epidemiology, 51 (1998): 443-460.

Ravsnskov, U. Hypothesis out-of-date. The diet-heart idea. Journal of Clinical Epidemiology, 55 (2002): 1,057-1,063.

Ravnskov, U, et al. Studies of dietary fat and heart disease. Science, 295 (2002): 1,464-1,465.

Taubes, G. The soft science of dietary fat. Science, 291 (2001): 2535-2541.

Zarraga, Ignatius, and Schwartz, Ernst. Impact of dietary patterns and interventions on cardiovascular health. Circulation, 114 (2006): 961-973.

Mente, Andrew, et al. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine, 169 (2009): 659-669.

Parikh, Parin, et al. Diets and cardiovascular disease: an evidence-based assessment. Journal of the American College of Cardiology, 45 (2005): 1,379-1,387.

Bray, G.A. Review of Good Calories, Bad Calories. Obesity Reviews, 9 (2008): 251-263. Reproduced at the Protein Power website of Drs. Michael and Mary Dan Eades.

Hooper, L., et al. Dietary fat intake and prevention of cardiovascular disease: systematic review. British Medical Journal, 322 (2001): 757-763.

Weinberg, W.C. The Diet-Heart Hypothesis: a critique. Journal of the American College of Cardiology, 43 (2004): 731-733.

Mozaffarian, Darius, et al. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. American Journal of Clinical Nutrition, 80 (2004): 1,175-1,184.

Related editorial: Knopp, Robert and Retzlaff, Barbara. Saturated fat prevents coronary artery disease? An American paradox. American Journal of Clinical Nutrition, 80 (2004): 1.102-1.103.

Yusuf, S., et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet, 364 (2004): 937-952. (ApoB/ApoA1 ratio was a risk factor for heart attack, so dietary saturated fat may play a role if it affects this ratio.)

Hu, Frank. Diet and cardiovascular disease prevention: The need for a paradigm shift. Journal of the American College of Cardiology, 50 (2007): 22-24.  (Dr. Hu de-emphasizes the original diet-heart hypothesis, noting instead that “. . . reducing dietary GL [glycemic load] should be made a top public health priority.:)

Oh, K., et al. Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the Nurses’ Health Study. American Journal of Epidemiology, 161 (2005): 672-679.

Parker, Steve. Time to abandon the diet-heart hypothesis? Advanced Mediterranean Diet Blog, May 1, 2009.

Parker, Steve. New study confirms the heart-healthy Mediterranean diet. Advanced Mediterranean Diet Blog, April 14, 2009. (Examination of the Mente study listed above.)

Selected References Supporting the Diet-Heart Hypothesis (by no means exhaustive)

Ascherio, A. Epidemiologic studies on dietary fats and coronary heart disease. American Journal of Medicine, 113 (supplement) (2002): 9S-12S.

Griel, Amy and Kris-Etherton, Penny. Beyond saturated fat: The importance of the dietary fatty acid profile on cardiovascular disease. Nutrition Reviews, 64 (2006): 257-262.  (Primarily a response to the Mozaffarian article above.)

Erkkila, Arja, et al. Dietary fatty acids and cardiovascular disease: An epidemiological approach. Progress in Lipid Research, 47 (2008): 172-187.